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细胞吸引

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To date, most research on DTCNNs has restricted to the stability of a system[17-19,37,38].Few papers consider the existence and attractability of periodic so-lutions.

迄今为止,大多数文献局限于研究离散细胞神经网络模型的稳定性,很少考虑离散时间细胞神经网络周期解的存在性及吸引性问题。

Some useful notations and definitions are give in this chapter.In Chapter 2,a class of discrete-time model of two-cell cellular neural networks with symmetric temptate are investigated. We obtain some results about the stability,asymptotic stability,the existence and attractability of 2-periodic solutions.

第三章讨论了反馈矩阵为非对称矩阵的二元离散细胞神经网络模型的稳定性与渐近稳定性、周期解的存在吸引性,除了得到系统稳定和存在2-周期解的相关结果外,还得到了系统在原点出现类似于Hopf分支的局部分支以及多个吸引4k-周期解的共同存在性。

It has several kinds of functions : It could accelerate blood coagulation; has chemotaxis to monocyte and neutrophil , could appeal to fibroblast and cartilage cell to move to the region of the injury, takes part in the signal transduction and activation in cell , and takes part in the growth and differentiation of cell and repair in trauma.

它的功能多样,能加速血液凝固,对单核细胞和中性粒细胞具有化学趋化作用,能吸引成纤维细胞和软骨细胞向损伤区域移动,参与细胞的信号传导与活化,细胞的生长及分化,创伤修复等一系列重要生理和病理过程。

During the curing process, first,to inject the Harmony No.1 at focus of patient directly to let medicine go inside of tumour, and after 24hours, the medicine will damage and dissolve the tumour cells; second, prick the area has been injected and make it as cinquefoil, use minus-pressure puller to drain gore of dead tumour cell out of body; third,to inject Harmony No.1 at focus again, then inject in mainline to clear virus and tumour cells haven't been formed in blood.

在对病人治疗过程,首先对肿瘤癌症病灶部位直接注射和谐一号核子注射液,使药物直接进入肿瘤内部,经过24小时药物对肿瘤细胞的杀死破坏及溶解;第二步,对注射处扎针,使其呈梅花状,用负压吸引器把含有坏死肿瘤细胞的瘀血排出体外;第三步,给病人病灶部位注射和谐一号注射液,再对病人注射静脉针液,用来清除血液中的病菌病毒及杀死血液中未形成的肿瘤细胞。

They are presented as a complex on the surface of the dendritic cell to attract the T-cells.

他们是作为一个复杂的表面,树突状细胞,以吸引T细胞。

The interaction of DAB and RB with SPM and the cells are exothermal and idiopathic, which contained the union of non-covalent bonds, such as electrostatic bond, hydrogen bond and van der Waals force. Moreover, most of DAB and RB were accumulated on the excellular membrane and walls, to hardly enter the cytoplasm.

结果表明, DAB, RB与SPM和细胞外膜有强烈的单分子层化学吸附,是自发的放热反应,主要通过电荷对吸引、氢键等非共价键结合在SPM和细胞外表面,且绝大部分DAB, RB积累、滞留在细胞膜壁上。

Membrane affinity quantified by IAM and liposome/buffer systems was a more efficient predicator of α values than hydrophobicity from n-octanol/buffer system. Consequently, not only hydrophobic force but also attractive polar extra-interactions involved in the binding to IAM and liposomal membranes but not in an n-octanol phase, ascribed to the binding process within AM. The binding to ordered lipid membrane in the larger part determined drugs'binding to AM intracellular compositions, and the ordered phospholipid plasma membrane was a potential site for drugs'binding in AM.

脂质体/水系统和磷脂膜色谱所测定的膜亲和性比正辛醇/水系统的疏水性更好的预测巨噬细胞内药物的α值,因此包含在磷脂膜色谱中但并不体现在正辛醇/水系统中药物与磷脂膜之间的额外吸引性极性作用力对药物在细胞内结合有着重要贡献;药物与有序磷脂膜的结合在很大程度上决定着药物与巨噬细胞内成分的结合,有序磷脂分子膜可能是巨噬细胞内部潜在的结合部位。

During the fertilization of angiosperms, the degenerated synergid induces a pollen tube to enter and break the pollen tube to release two sperm cells, which fuse with the egg and central cell.

在受精过程中,助细胞吸引花粉管向雌配子体生长,并接受花粉管长入细胞程序死亡助细胞中。接下来的花粉管停止生长和花粉管顶端破裂释放出2个精细胞的过程可能也依赖于助细胞。

There were significant differences between all the experimental groups and the control group (F=193.25, P<0.01). Conclusions IL-1β and TNF-α induce a strong expression of MCP-1 mRNA and protein in HUVECs. Both cytokines may be involved in the atherogenesis by inducing the liberation of MCP-1 by endothelial cells and increasing the recruitment of monocytes into the subendothelial space.

IL-1β和TNFα均能显著增强内皮细胞MCP-1 mRNA和蛋白的表达,提示它们通过诱导内皮细胞产生MCP-1,吸引单核细胞迁入动脉内膜而参与动脉粥样硬化的发生和发展。

Furthermore, we found that the Sema3F-triggered growth cone attraction was abolished by inhibition of the cGMP signaling pathway but not by inhibition of the cAMP signaling pathway, and the attraction was suppressed when elevating the intracellular cGMP level.

而且,在组织块共培养中,分泌Sema3F的细胞团能使小脑颗粒细胞偏向它迁移。我们发现Sema3F的吸引性作用在cGMP信号通路被抑制时受阻断,在细胞内cGMP水平增加时被削弱。

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然而,正如其名字所指出的那样,CD盘不能写,也不能用任何方式改变其内容。

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